Mari Aksnes

Stipendiat - Geriatrisk avdeling

English version of this page

E-post mari.aksnes@medisin.uio.no

Telefon +47 47303885

Brukernavn

Besøksadresse Kirkeveien 166 Bygg 20 0450 Oslo

Postadresse OUS HF Ullevål sykehus Postboks 4956 Nydalen 0424 Oslo

Andre tilknytninger Det medisinske fakultet (Student)

Last ned visittkort

Faglige interesser

Jeg er interessert i biologiske endringer ved nevrodegenerasjon og hvordan disse utvikler seg i, og påvirker funksjonen av, hjernen. Forståelse av disse endringene kan på sikt bidra til å identifisere, behandle og forhindre nevrodegenerative sykdommer som Alzheimers sykdom.

I mitt PhD-prosjekt forsker jeg på biomarkører for Alzheimers sykdom, biologiske endringer assosiert med sykdommen som kan bidra til bedre og tidligere diagnostikk.

Bakgrunn

Utdannelse

2018 -
Universitetet i Oslo, PhD stipendiat i geriatri og nevrovitenskap
2015-2017
Norges teknisk-naturvitenskapelige universitet, MSc i nevrovitenskap
"Effect of cerebrospinal fluid from patients with Alzheimer's disease on protein expression in the hippocampal region of a transgenic rat model of Alzheimer's disease"
2012-2015
University of Durham, BSc i psykologi
"The effects of forced fixation on diagnostic and non-diagnostic facial features on emotion identification: Exploring the association with callous-unemotional traits, alexithymia and empathy"

Arbeidserfaring

2018 - Universitet i Oslo,
PhD-stipendiat i geriatri og nevrovitenskap i demensforskningsgruppen på Ullevål
2018 Oslo Universitetssykehus, Maria Korsnes' forskningsgruppe
Forskningsassistent
2017 - 2018 Forskerfabrikken
Kursleder forskerkurs for barn
2017 - Bjørknes Høyskole
Veileder og sensor

Publikasjoner

Vitenskapelige artikler og bokkapitler

Aksnes, Mari; Müller, Ebba Gløersen; Tiiman, Ann; Edwin, Trine Holt; Terenius, Lars; Rootwelt-Revheim, Mona-Elisabeth; Vukojevic, Vladana; Bogdanovic, Nenad & Knapskog, Anne Brita (2020). Amyloidogenic nanoplaques in cerebrospinal fluid: Relationship to amyloid brain uptake and clinical Alzheimer's disease in a memory clinic cohort. Journal of Alzheimer's Disease. ISSN 1387-2877. 77(2), s 831- 842 . doi: 10.3233/JAD-200237 Vis sammendrag
Background: Aggregation of amyloid-β (Aβ) is an early pathological event in Alzheimer’s disease (AD). Consequently, measures of pathogenic aggregated Aβ are attractive biomarkers for AD. Here, we use a recently developed Thioflavin-T-Fluorescence Correlation Spectroscopy (ThT-FCS) assay to quantify structured ThT-responsive protein aggregates, so-called nanoplaques, in the cerebrospinal fluid (CSF). Objective: The overall aim of this work was to assess whether ThT-FCS determined CSF nanoplaque levels could predict amyloid brain uptake as determined by 18F-Flutemetamol PET analysis. Further, we assess whether nanoplaque levels could predict clinical AD. Methods: Nanoplaque levels in the CSF from 54 memory clinic patients were compared between sub-groups classified by 18F-Flutemetamol PET as amyloid-positive or amyloid-negative, and by clinical assessment as AD or non-AD. Results: Nanoplaque levels did not differ between amyloid groups and could not predict brain amyloid uptake. However, nanoplaque levels were significantly increased in patients with clinical AD, and were significant predictors for AD when adjusting for age, sex, cognitive function, and apolipoprotein E (APOE) genotype. Conclusion: The concentration of nanoplaques in the CSF differentiates patients with clinical AD from non-AD patients.

Publisert 14. jan. 2019 11:48 - Sist endret 13. juni 2019 11:37